Biomedical subjects
Publications and source records attributed to R Korbut.
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Recently two local hormones, thromboxane A2 (TXA2) and prostacyclin (PGI2) have been discovered. These hormones are labile metabolites of arachidonic acid. TXA2 is generated by blood platelets, while PGI2 is produced by vascular endothelium. TXA2 is a potent vasoconstrictor. It also initiates the release reaction, followed by platelet aggregation. PGI2 is a vasodilator, especially potent in coronary circulation. It also inhibits platelet aggregation by virtue of stimulation of platelet adenyl cyclase. Common precursors for both hormones are cyclic endoperoxides PGG2 and PGH2, being formed by cyclooxygenation of arachidonic acid. This last enzymic reaction is more efficient in platelets than in vascular endothelium, and therefore the generation of PGI2 by vasuclar wall is accelerated by an interaction between platelets and endothelial cells. During this interaction platelets supply the endothelial PGI2 synthetase with their cyclic endoperoxides. The newly formed PGI2 repels the platelets from the intima. When PGI2 synthetase is irreversibly inactivated by low concentration of lipid peroxides, then the platelets are not rejected but stick to the endothelium, generate TXA2 and mature thrombi are formed. A balance between formation and release of PGI2, TXA2 and/or cyclic endoperoxides in circulation is of utmost importance for the control of intra-arterial thrombi formation and possibly plays a role in the pathogenesis of atherosclerosis.
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During anaphylactic reactions there are released thromboxane A2 and/or prostaglandin-like substances from perfused guinea pig lungs and from incubated fragments of guinea pig mesentery. Prostaglandin-like substances appear also in mixed venous blood of anaesthetized cats following an intravenous injection of rabbit blood. These release reactions are reduced or abolished both by indomethacin and by hydrocortisone.
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1. An Amberlite XAD-2 column in a heated (37 degrees C) jacket was incorporated in between two banks of bioassay organs superfused with Krebs bicarbonate solution in cascade. The column removed prostaglandins, E1, E2 and F2alpha and also rabbit aorta contracting substance (RCS) and possibly slow reacting substance of anaphylaxis (SRS-A). 2. The column gave free passage to histamine in concentrations up to 3000 ng/ml. The method described improved the accuracy of histamine bioassay in the.presence of prostaglandins.
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Infusion of norephinephrine (NE) (1 - 3 mug/ml/min) into the isolated mesenteric vascular preparation of rabbit resulted in a rise in perfusion pressure, which was associated with the release of prostaglandin E-like substance (PGE) at a concentration of 2.81 +/- 0.65 ng/ml in terms of PGE2. Indomethacin (3 mug/ml) abolished the NE-induced release of PGE. Arachidonic acid (0.2 mug/ml) in the presence of indomethacin did not restore the NE-induced release of PGE. Hydrocortisone (10 - 30 mug/ml) and dexamethasone (2 - 5 mug/ml) also inhibited the NE-induced release of PGE. The inhibitory action of both corticosteroids was abolished by arachidonic acid (0.2 mug/ml). Antigen-induced release of a prostaglandin-like substance (PGs) (43.1 +/- 3.8 ng/ml in terms of PGE2 and a rabbit aorta contracting substance (RCS) from perfused lungs of sensitized guinea pigs was completely abolished by indomethacin (5 mug/ml) or by hydrocortisone (100 mug/ml). Indomethacin, however, increased histamine release up to 280% of the control level, which was 470 +/- 54 ng/ml, while hydrocortisone diminished histamine release down to 30% of the control level. A superimposed infusion of arachidonic acid (1 mug/ml) into the pulmonary artery reversed the hydrocortisone-induced blockade of the release of RCS and PGs. It may be concluded that corticosteroids neither inhibit prostaglandin synthetase nor influence prostaglandin transport through the membranes but they do impair the availability of the substrate for the enzyme.
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An iv injection of E. coli endotoxin (10--15 mg/kg) produced biphasic hypotensive reaction in cats. The second phase of hypotension developed 5--10 min after the administration of endotoxin and was paralleled by an appearance of a substance contracting the chick rectum and rat colon which were bathed in mixed venous blood. On the basis of differential sensitivity of the assay organs to prostaglandins it was concluded that a prostaglandin E-like substance (PGEs) was released. Its peak concentration in blood was 1--3-5 ng/ml in terms of PGE2-like activity. Indomethacin (10 mg/kg) interrupted the liberation of PGEs into blood and at the same time a slow but steady increase in arterial blood pressure occured. The amelioration of endotoxin hypotension by indomethacin was abolished by an infusion of PGE2 at a rate of 20--100 ng/kg/min. It is suggested that the second phase of endotoxin hypotension in cats is mediated by a release of PGEs.
A column filled with activated aluminium oxide is incorporated into the bioassay system of Vane in which a rat stomach strip, a chick rectum and a rat colon are superfused in cascade. The absorbance of catecholamines by the column and the passage of prostaglandins through the column are almost 100%. This modification of Vane's technique enables PGE1, PGE2, PGF2, F2a to be estimated at concentrations as low as 0-5--1-0 ng/ml in the presence of catecholamines at a concentration as high as 50 ng/ml. Using this method we have demonstrated the release of small amounts (2 ng/ml) of an endogenous PGE-like substance from rabbit ear vessels contracted by an infusion of norepinephrine (500 ng/ml/min).
It is reported that noradrenaline-induced vasoconstriction initiates generation of prostaglandins of the E series by vasculas walls. These endogenous prostaglandins attenuate the vasoconstrictor effect of noradrenaline. Inhibitors of prostaglandin biosynthesis (indomethacin, mefenamic acid) abolish acute tolerance to noradrenaline infusions and counteract hypotension which is induced in cats by injection of endotoxin or by injection of rat blood.
The aim of this study was to examine the effect of ketoprofen used in preemptive analgesia on the intensity of pain and requirement for analgesics in the perioperative period. Sixty patients scheduled for elective lumbar disc prolapse surgery were randomly divided into two groups. In the PRE group (n = 30) ketoprofen was administered one hour before incision. In the POST group ( n = 30) ketoprofen was used immediately after the surgery. The operation was performed under general anesthesia. Postoperative analgesia was realized by NCA (Nurse Controlled Analgesia) and the "required" dose of ketoprofen was 100 mg. After the operation, pain intensity was measured using visual-analog scale (VAS), ketoprofen requirements, the time to the first dose of ketoprofen, and levels of prostaglandin E(2) (PEG(2)) in blood serum were compared. There were no differences between the groups in the VAS pain scores, and levels of PGE(2) in blood serum. However, in patients of PRE group who had received preemptive analgesia, a significantly lower total consumption of ketoprofen, as compared with POST group, was observed between 12th and 36th postoperative hours. It was also found that the time which elapsed between the end of the operation and the first NCA activation was significantly shorter in the PRE group, as compared with the POST group. The results of our study confirm the possibility of modifying the nociception process in the perioperative period through preemptive analgesia by ketoprofen.
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